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UNDERSTANDING RECOVERY: A WOUND HEALING

MODEL
by Dave Staplin

To understand and study the process of muscle recovery and repair, it is useful
to develop a MODEL. Modeling the biochemical reactions to stress and the
observed effects such as soreness allow for a better understanding of the events
and TIME COURSE necessary for muscle recovery. Such a model comes from the
study of the wound healing process; particularly the inflammatory reponse (7,9).
Whenever muscle cells are subjected to high intensity anaerobic training stress,
damage occurs at the cellular level (1-4,7-9). The DEGREE of damage depends
upon the degree of intensity--the higher the intensity, the greater the damage
(2,4,5,7,9,10). It is the process of healing this damage which then makes the
muscle cell larger and stronger(2,9).

Recovery from training stress requires a number of steps; each of which must
proceed to completion UNINTERRUPTED for COMPLETE recovery and adaptive
response (7,9). While the exact mechanisms are unclear at the present time and
subject to further research and clarification, it is thought that acute
inflammation is the initial response to muscle cell damage (7,9,10). This is
especially the case where high intensity eccentric work is performed such as
Negative Training, Hyper Training or when accentuating the Lowering of the
weight during standard repetitions. Delayed-onset muscle soreness is thought to
be one of the effects of this acute inflammatory response as well (1-8,10). This
sequence of events occurs in the following manner and time:

1. Connective and/or contractile tissue (muscle cell) damage occurs during

intense muscular contraction, particularly eccentric action (1-10).
2. Within the first 24 hours, levels of neutrophils (white blood cells which
respond to injury) increase and migrate to the site of injury or exercise
trauma (1,6,9).
3. At the same time, lysosomal enzymes which digest and break down
damaged tissue are released and this breakdown activity commences
(3,6,8,9,10).
4. Macrophages (cells which aid lysosomes and synthesize a variety of
chemicals in response to inflammation) begin to accumulate around 24
hours and continue to do so for up to several days. One of the chemicals
these cells secrete, PGE2, is believed to make nerves , more sensitive to
pain and may help explain soreness sensations starting 24 hours or so
after exercise, and lasting for as long as 7 or more days (1-7,9,10).

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5. This inflammatory response causes further damage to the affected area

and may continue for several days beyond imposition of the INITIAL
training stress damage (1,6,7,9).
6. Once these initial inflammatory responses (steps 1-5) are completed, then
signs of the BEGINNINGS of tissue regeneration (rebuilding of the muscle)
can be observed (4,7,9).

The muscle cell must first rebuild to normal levels of structure and function and
then, only then, and only IF allowed FURTHER TIME, will it supercompensate and
build up to levels GREATER than before. The next question is: How long does this
ENTIRE process take?

It must be remembered that the severity of response and so the time necessary
to complete it vary according to the degree of trauma or in this case, the
intensity of the work, the muscle has been subjected to (2,4,5,10). Numerous
studies have examined this response process, especially with eccentric
contractions (1-10). The time course for completion of the above 6 steps ranges
from 5 days to over 6 weeks (1-10)! This has profound implications regarding
FREQUENCY of training! The more intense your training, the longer you must
allow for recovery. If you add 50% to the weight you normally use for high
intensity repetitions and then proceed to perform NEGATIVE repetitions, you
have just dramatically increased the stress and therefore the TIME necessary for
the muscle to recover. One concrete training example may help further clarify
these ideas.

From mid-July to mid-October 1997, my training partner and I increased our

Squat and Deadlift poundages 49% and 70%, respectively. We used standard
repetition protocol--2 seconds concentric (raising) and 4 second eccentric
(lowering). We terminated sets when no more full-range, unassisted reps were
possible. In other words, we performed no Forced Reps, Negatives or any other
technique which would have increased the intensity of the sets. Further, we had
been performing only 2 sets per workout every 7 days on Mike's Consolidation
Routine.

By early November, we had experienced 2 consecutive workouts with no further

progress in any of our sets. We then took 23 days off. We returned to the gym
and we were now able to add 10% to the Squat poundages for the same number
of reps as our previous squat workout AND we had not performed squats for 30
days!

At first, this may seem beyond belief--an absolute impossibility! Not, however, if
you understand recovery from the standpoint of the inflammatory response and
recovery model outlined in steps 1-6 above. It is important to never forget that
high intensity anaerobic weight training stress is a study properly subsumed
under the heading of MEDICAL SCIENCE. As such, medical science can teach us

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UNDERSTANDING RECOVERY: A WOUND HEALING MODEL https://www.mikementzer.com/wound1_0606.html

much, but as pioneers in the field of high intensity, anaerobic exercise, so too
can we teach medical science much!

1) Clarkson, PM, Nosaka, K. Muscle function after exercise-induced muscle

damage and rapid adaptation. Medicine and Science in Sports and Exercise.
Vol.24, No.5, 512-20, 1992

2) Clarkson, PM, Tremblay, I. Exercise-induced muscle damage, repair and

adaptation in humans. Journal of Applied Physiology. Vol.65, No.1, 1-6, 1988

3) Friden, J.,et al Myofibrillar damage following intense eccentric exercise in

man. International Journal of Sports Medicine. Vol.24, No.3, 170-176,1983

4) Golden, CL, Dudley, GA., Strength after bouts of eccentric or concentric

actions. Medicine and Science in Sports and Exercise. Vol.24, No.8, 926-33, 1992

5) Howell, JN, Chleboun,G., Muscle stiffness, strength loss, swelling and soreness
following exercise-induced injury to humans. Journal of Physiology 464, 183-96,
1993

6) Jones, DA, Newham, JM., et al, Experimental human muscle damage:

morphological changes in relation to other indices of damage. Journal of
Physiology 375, 435-48, 1986

7) Mishra, DK, Friden, J., et al Anti-inflammatory medication after muscle injury.

Journal of Bone and Joint Surgery, Vol. 77-A, No.10, 1510-19, 1995 8) Newman,
DJ, Jones, DA., Repeated high-force eccentric exercise: effects on muscle pain
and damage. Journal of Applied Physiology Vol.4, No.63, 1381-86, 1987

9) Smith, LL. Acute inflammation: the underlying mechanism in delayed onset

muscle soreness? Medicine and Science in Sports and Exercise Vol. 23, No.5,
542-51, 1991

10) Tiidus, PM, Ianuzzo, DC., Effects of intensity and duration of muscular
exercise on delayed soreness and serum enzyme activities. Medicine and
Science in Sports and Exercise Vol. 15, No.6, 461-5, 1983

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